Nutritional Neuroscience,
Journal Year:
2023,
Volume and Issue:
27(8), P. 870 - 886
Published: Sept. 20, 2023
ABSTRACTParkinson's
disease
(PD)
is
a
chronic
neurodegenerative
(NDD)
due
to
the
degeneration
of
dopaminergic
neurons
(DNs)
in
substantia
nigra
(SN).
PD
characterized
by
diverse
motor
symptoms
such
as
rigidity,
resting
tremors,
and
bradykinesia,
non-motor
cognitive
dysfunction
sleep
disturbances.
Vitamin
D
(VD),
VD
receptor
(VDR),
metabolites
are
present
brain
play
role
maintaining
development,
differentiation,
functions
DNs.
VDRs
exert
protective
effects
against
neuropathology
modulating
functional
capacity
DNs
neurotransmission
SN.
In
virtue
its
anti-inflammatory
antioxidant
activities,
could
be
effective
prevention
treatment
PD.
exerts
neuroprotective
effect
reducing
oxidative
stress
mitochondrial
dysfunction,
increasing
autophagy
brain-derived
neurotrophic
factor
(BDNF).
Low
serum
level
connected
with
development
dementia
The
VD-mediated
augmenting
interrelated
safeguarding
synaptic
plasticity
modulation
neurotransmitter
release.
deficiency
linked
severity
olfactory
which
precedes
progression
symptomatic
However,
precise
remains
unidentified,
there
conflict
about
whether
can
ameliorate
or
not.KEYWORDS:
Parkinson's
diseaseVitamin
DVD
receptorBDNFsubstantia
nigraAutophagyOxidative
stressdopaminergic
AcknowledgementsNot
applicable.Authors'
contributionsAAH
conceptualized
manuscript,
wrote,
edited,
reviewed
main
text
approved
final
edition
manuscript.Disclosure
statementNo
potential
interest
was
reported
author(s).Additional
informationFundingThe
author(s)
no
funding
associated
work
featured
this
article.
Parkinson's
disease
(PD)
is
a
progressive
neurodegenerative
brain
due
to
degeneration
of
dopaminergic
neurons
(DNs)
presented
with
motor
and
non-motor
symptoms.
PD
symptoms
are
developed
in
response
the
disturbance
diverse
neurotransmitters
including
γ-aminobutyric
acid
(GABA).
GABA
has
neuroprotective
effect
against
neuropathology
by
protecting
DNs
substantia
nigra
pars
compacta
(SNpc).
It
been
shown
that
GABAergic
linked
progression
neurotransmission
necessary
pathway
for
normal
sleep
patterns,
thus
deregulation
could
be
potential
cause
disorders
PD.
Neurochemical Research,
Journal Year:
2023,
Volume and Issue:
48(11), P. 3255 - 3269
Published: July 13, 2023
Abstract
Multiple
sclerosis
(MS)
is
an
autoimmune
demyelinating
neurodegenerative
disease
of
the
central
nervous
system
(CNS)
due
to
injury
myelin
sheath
by
immune
cells.
The
clotting
factor
fibrinogen
involved
in
pathogenesis
MS
triggering
microglia
and
progress
neuroinflammation.
Fibrinogen
level
correlated
with
severity;
consequently,
inhibition
cascade
may
reduce
neuropathology.
Thus,
this
review
aimed
clarify
potential
role
how
targeting
affects
Accumulation
CNS
occur
independently
or
disruption
blood–brain
barrier
(BBB)
integrity
MS.
acts
as
transduction
increases
activation
which
induces
progression
inflammation,
oxidative
stress,
neuronal
injury.
Besides,
brain
impairs
remyelination
process
inhibiting
differentiation
oligodendrocyte
precursor
These
findings
proposed
that
associated
neuropathology
through
interruption
BBB
integrity,
induction
neuroinflammation,
demyelination
suppressing
oligodendrocytes.
Therefore,
and/or
CD11b/CD18
receptors
metformin
statins
might
decrease
In
conclusion,
expression
pro-inflammatory
effect
on
Journal of Cellular and Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
28(10)
Published: May 1, 2024
Parkinson's
disease
(PD)
is
a
neurodegenerative
disorder
of
the
brain
and
manifested
by
motor
non-motor
symptoms
because
degenerative
changes
in
dopaminergic
neurons
substantia
nigra.
PD
neuropathology
associated
with
mitochondrial
dysfunction,
oxidative
damage
apoptosis.
Thus,
modulation
apoptosis
growth
factors
could
be
novel
boulevard
management
PD.
Brain-derived
neurotrophic
factor
(BDNF)
its
receptor
tropomyosin
kinase
type
B
(TrkB)
are
chiefly
involved
neuropathology.
BDNF
promotes
survival
nigra
enhances
functional
activity
striatal
neurons.
Deficiency
TrkB
triggers
degeneration
accumulation
α-Syn
As
well,
BDNF/TrkB
signalling
reduced
early
phase
Targeting
specific
activators
may
attenuate
this
review
aimed
to
discuss
potential
role
against
In
conclusion,
decreased
linked
severity
long-term
complications.
Activation
Diabetes Obesity and Metabolism,
Journal Year:
2024,
Volume and Issue:
26(8), P. 3031 - 3044
Published: May 27, 2024
Abstract
Depression
is
a
mood
disorder
that
may
increase
risk
for
the
development
of
insulin
resistance
(IR)
and
type
2
diabetes
(T2D),
vice
versa.
However,
mechanistic
pathway
linking
depression
T2D
not
fully
elucidated.
The
aim
this
narrative
review,
therefore,
was
to
discuss
possible
link
between
T2D.
coexistence
twice
as
great
compared
occurrence
either
condition
independently.
Hyperglycaemia
dyslipidaemia
promote
incidence
by
enhancing
inflammation
reducing
brain
serotonin
(5‐hydroxytryptamine
[5HT]).
Dysregulation
signalling
in
impairs
5HT
signalling,
leading
depression.
Furthermore,
associated
with
hyperglycaemia
poor
glycaemic
control.
Psychological
stress
In
conclusion,
could
be
potential
factor
through
induction
inflammatory
reactions
oxidative
affect
neurotransmission.
addition,
chronic
induce
dysregulation
hypothalamic–pituitary–adrenal
axis
circulating
cortisol
levels,
which
triggers
IR
Autophagy,
Journal Year:
2024,
Volume and Issue:
20(7), P. 1473 - 1482
Published: Feb. 12, 2024
Myasthenia
gravis
(MG)
is
an
autoimmune
disease
of
the
neuromuscular
junction
(NMJ)
that
results
from
autoantibodies
against
nicotinic
acetylcholine
receptors
(nAchRs)
at
NMJs.
These
are
mainly
originated
autoreactive
B
cells
bind
and
destroy
nAchRs
NMJs
preventing
nerve
impulses
activating
end-plates
skeletal
muscle.
Indeed,
immune
dysregulation
plays
a
crucial
role
in
pathogenesis
MG.
Autoreactive
increased
MG
due
to
defect
central
peripheral
tolerance
mechanisms.
As
well,
T
augmented
diversion
regulatory
(T
Molecular Neurobiology,
Journal Year:
2024,
Volume and Issue:
61(9), P. 7092 - 7108
Published: Feb. 17, 2024
Abstract
Parkinson’s
disease
(PD)
is
a
progressive
neurodegenerative
of
the
brain
due
to
degeneration
dopaminergic
neurons
in
substantia
nigra
(SN).
Glycogen
synthase
kinase
3
beta
(GSK-3β)
implicated
pathogenesis
PD.
Therefore,
purpose
present
review
was
revise
mechanistic
role
GSK-3β
PD
neuropathology,
and
how
inhibitors
affect
neuropathology.
GSK-3
conserved
threonine/serine
protein
that
intricate
regulation
cellular
anabolic
catabolic
pathways
by
modulating
glycogen
synthase.
Over-expression
also
interconnected
with
development
different
diseases.
However,
underlying
mechanism
neuropathology
not
fully
clarified.
induces
triggering
mitochondrial
dysfunction
oxidative
stress
SN.
NF-κB
NLRP3
inflammasome
are
activated
response
dysregulated
leading
neuronal
injury.
Higher
expression
early
stages
might
contribute
reduction
neuroprotective
brain-derived
neurotrophic
factor
(BDNF).
Thus,
may
be
effective
reducing
inflammatory
disorders
which
associated
Journal of Cellular and Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
28(12)
Published: June 1, 2024
Abstract
Parkinson
disease
(PD)
is
one
of
the
most
common
neurodegenerative
diseases
brain.
Of
note,
brain
renin‐angiotensin
system
(RAS)
intricate
in
PD
neuropathology
through
modulation
oxidative
stress,
mitochondrial
dysfunction
and
neuroinflammation.
Therefore,
RAS
by
angiotensin
receptor
blockers
(ARBs)
angiotensin‐converting
enzyme
inhibitors
(ACEIs)
may
be
effective
reducing
risk
neuropathology.
It
has
been
shown
that
all
components
including
peptides
enzymes
are
present
different
areas.
Brain
plays
a
critical
role
regulation
memory
cognitive
function,
controlling
central
blood
pressure.
However,
exaggerated
implicated
pathogenesis
PD.
Two
well‐known
pathways
recognized
including;
classical
pathway
which
mainly
mediated
AngII/AT1R
detrimental
effects.
Conversely,
non‐classical
mostly
ACE2/Ang1‐7/MASR
AngII/AT2R
beneficial
effects
against
Exaggerated
affects
viability
dopaminergic
neurons.
fundamental
mechanism
was
not
fully
elucidated.
Consequently,
purpose
this
review
to
disclose
mechanistic
In
addition,
we
try
revise
how
ACEIs
ARBs
can
developed
for
therapeutics
Neuropsychopharmacology Reports,
Journal Year:
2024,
Volume and Issue:
44(3), P. 639 - 649
Published: July 29, 2024
Abstract
Neurodegenerative
diseases
(NDs)
such
as
Alzheimer
disease
(AD)
and
Parkinson
(PD)
are
group
of
affecting
the
central
nervous
system
(CNS)
characterized
by
progressive
neurodegenerations
cognitive
impairment.
Findings
from
different
studies
highlighted
beneficial
detrimental
effects
serum
uric
acid
on
development
progression
NDs.
Therefore,
this
mini‐review
aims
to
discuss
The
neuroprotective
effect
is
mainly
related
antioxidant
which
alleviates
oxidative
stress‐induced
neurodegeneration
in
AD
PD.
However,
long‐term
hyperuricemia
prompts
for
Hyperuricemia
associated
with
impairment
dementia,
gout
increases
dementia
risk.
In
addition,
can
cause
cerebral
vascular
injury
a
risk
factor
Taken
together,
relationship
between
NDs
remains
conflicting.
Hence,
preclinical
clinical
indicated
regard.